Interpretive Summary: Genetic markers within mu-calpain, calpastatin, and growth hormone receptor genes previously associated with beef quality traits did not always have animals with two copies of the rare alleles in previous studies. Selection was performed to ensure observations with all three genotypes (2 copies of common allele, heterozygotes, and 2 copies of rare allele) could be evaluated for their effects on beef quality traits. This work confirms the importance of mu-calpain and calpastatin genetic markers for changing average beef tenderness. It also identifies the mode of inheritance as additive, with no interaction between mu-calpain and calpastatin on beef tenderness. Beyond changes in the average beef tenderness associated with the genetic markers, we also identified differences in variability of beef tenderness associated with genetic markers. This provides more information about the probability of a particular animal producing tough beef, which may not be acceptable to a consumer. Information about the effect size, mode of inheritance, and lack of interaction between genetic markers are important for developing breeding and management systems to be used by cattle producers to produce tender, high quality beef desirable to U.S. and international consumers.

Technical Abstract: Genetic marker effects and interactions are estimated with poor precision when minor marker allele frequencies are low. An Angus population was subjected to marker assisted selection for multiple years to increase divergent haplotype and minor marker allele frequencies to 1) estimate effect size and mode of inheritance for previously reported SNP on targeted beef carcass quality traits; 2) estimate effects of previously reported SNP on nontarget performance traits; and 3) evaluate tenderness SNP specific residual variance models compared to a single residual variance model for tenderness. Divergent haplotypes within µ-calpain (CAPN1), and SNP within calpastatin (CAST) and growth hormone receptor (GHR) were successfully selected to increase their frequencies. Traits evaluated were birth BW, weaning BW, final BW, fat thickness, LM area, USDA marbling score, yield grade, slice shear force (SSF), and visible and near infrared predicted slice shear force. Both CAPN1 and CAST exhibited additive (P < 0.001) modes of inheritance for SSF and neither exhibited dominance (P >/_ 0.19). Furthermore, the interaction between CAPN1 and CAST for SSF was not significant (P = 0.55). Estimated additive effects of CAPN1 (1.049 kg) and CAST (1.257 kg) on SSF were large in this study. Animals homozygous for tender alleles at both CAPN1 and CAST would have 4.61 kg lower SSF (38.6% of the mean) than animals homozygous tough for both markers. There was also an effect of CAST on yield grade (P < 0.02). The tender CAST allele was associated with more red meat yield and less trimmable fat. There were no significant effects (P >/_ 0.23) for GHR on any of the traits evaluated in this study. Furthermore, CAST specific residual variance models were found to fit significantly better (P < 0.001) than single residual variance models for SSF, with the tougher genotypes having larger residual variance. Thus, the risk of a tough steak from the undesired CAST genotype is increased through both an increase in mean and an increase in variation. This work confirms the importance of CAPN1 and CAST for tenderness in beef, provides a new effect of CAST on beef tenderness, and questions the utility of GHR as a selection marker for beef quality.